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1 produced no reduction in the severity of the audiogenic seizure.
2 areas for the initiation and propagation of audiogenic seizures.
3 relate with susceptibility and resistance to audiogenic seizures.
4 that is critical in the initiation of reflex audiogenic seizures.
5 rotein synthesis, exaggerated mGluR-LTD, and audiogenic seizures.
6 fore unrecognized specific susceptibility to audiogenic seizures.
7 der, including sudden unexplained deaths and audiogenic seizures.
8 behaviour, defective social interaction and audiogenic seizures.
9 e functions, and increased susceptibility to audiogenic seizures.
10 These mice were also found to be prone to audiogenic seizures.
11 s was sufficient to convey susceptibility to audiogenic seizures.
12 vely in somatostatin (SST) interneurons have audiogenic seizures.
15 initiation site in the neuronal network for audiogenic seizure (AGS) in rats undergoing ethanol with
16 (IC) central nucleus (ICc), is critical for audiogenic seizure (AGS) initiation in the genetically e
19 implicated in the neuronal network for these audiogenic seizures (AGS) in animals undergoing ETX.
20 pathway is also implicated in the network of audiogenic seizures (AGS) in genetically epilepsy-prone
22 iculus (DLSC) play a role in the network for audiogenic seizures (AGS) in genetically epilepsy-prone
23 cantly reduces the incidence and severity of audiogenic seizures (AGS) in the Fmr1(-/y) mouse, as doe
24 us studies indicate that daily repetition of audiogenic seizures (AGS) leads to audiogenic 'kindling'
25 In rodents, ETX results in susceptibility to audiogenic seizures (AGS), and the DLSC are implicated a
26 t-ictal analgesia occurs in GEPRs, following audiogenic seizures (AGS), and whether this analgesia in
27 (GEPR-3s) exhibits generalized onset clonic audiogenic seizures (AGS), but following repetitive AGS
28 ucture in the requisite neuronal network for audiogenic seizures (AGS), which is confined to the brai
34 controls to flurothyl, PTZ, kainic acid, and audiogenic seizures and enhanced sensitivity (i.e., seiz
35 ependent LTD, neocortical hyperexcitability, audiogenic seizures, and altered behaviors, including an
36 mice exhibited impaired motor coordination, audiogenic seizures, and brainstem neurodegeneration.
37 tigation studied the mode of inheritance for audiogenic seizures by crossing the Frings mouse with th
38 3ahl variant may account for the hearing and audiogenic seizure differences observed between Frings a
43 res evoked by gamma-butyrolactone (GBL), and audiogenic seizures in genetically epilepsy-prone rats.
44 ice all exhibit an enhanced tendency to have audiogenic seizures in response to white noise stimuli a
46 scribe a mutation in a novel gene underlying audiogenic seizures in the Frings mouse, providing a val
50 loss (age-related hearing loss 5, ahl5) and audiogenic seizures (juvenile audiogenic monogenic seizu
54 mg/kg had no effect in 4/4 rats made acutely audiogenic seizure-prone by infusion of bicuculline into
55 entricular (i.c.v.) administration of GRP to audiogenic seizure-prone DBA/2 mice prior to exposure to
58 acoustic hypersensitivity and propensity for audiogenic seizures, suggesting altered auditory respons
59 trols and a group of animals displaying high audiogenic seizure susceptibility (100% AGS) (HAGS), and
60 e human ortholog of the gene responsible for audiogenic seizure susceptibility in Frings and BUB/BnJ
61 ve GSK3 promotes locomotor hyperactivity and audiogenic seizure susceptibility in FX mice, raising th
64 receptor 1), also known as MASS1 (monogenic audiogenic seizure susceptible 1), is an orphan G protei
65 rings strain, 391 of the 836 N2 progeny were audiogenic seizure susceptible, a finding consistent wit
66 the seizure gene, named mass1 for monogenic audiogenic seizure susceptible, to an approximately 3.6
68 ological dysfunction, neurodegeneration, and audiogenic seizures that manifest beginning in early adu
69 eurological applications, such as preventing audiogenic seizures that originate in the auditory midbr